Researchers who have assembled a trove of genetic and medical data on 100,000 northern Californians unveiled their initial findings here this week at the annual meeting of the American Society of Human Genetics (ASHG). The effort, which may be the largest such "biobank" in the United States, has already yielded an intriguing connection between mortality and telomeres, the protective DNA sequences that cap chromosome ends, and found new links between genetic variants and disease traits. And that's just the beginning, say the biobank's curators at Kaiser Permanente (KP), the giant health care organization.

The KP biobank, which will draw on a variety of anonymized data drawn from patients' medical records—from medications to brain images—is also open to outside researchers. "This is obviously a very rich set of data that we want to be widely used," Schaefer says. Her team will deposit a data set in dbGaP, an NIH database for sharing SNPs data sets. Researchers can also apply to collaborate with the Kaiser Permanente team. Exactly how it will be used will be "up to the creativity and ingenuity of lots of people," Risch says. For example, researchers could use geographical databases on air pollution to look for links between illness and pollution. The biobank may also grow—a total of 200,000 KP members have donated biological samples and 430,000 have filled out a survey saying they're interested in participating.

"It's great. They have a huge data set," says Aravinda Chakravarti, a human geneticist at Johns Hopkins University in Baltimore, Maryland, who is already discussing collaboration with KP. However, he expressed reservations about the general push to link genes to diseases—at the ASHG meeting, many talks discussed efforts to sequence part or all of peoples' genomes to uncover rarer disease genes than SNP studies can find. "The problem in our field is that we're making lists" of disease genes, Chakravarti says. Like some others, he would like to see more emphasis on understanding the biology of how those genes function and cause illness.

A team of researchers working at Harvard University has taken yet another step towards bringing to life a reasonable facsimile of a woolly mammoth—a large, hairy elephant-like beast that went extinct approximately 3,300 years ago. The work by the team has not been published as yet, because as team lead George Church told The Sunday Times, recently, they believe they have more work to do before they write up their results.

Church is quick to point out that his team is not cloning the mammoth, instead they are rebuilding the genome of the ancient animal by studying its DNA, replicating it and then inserting the copy into the genome of an Asian elephant—the closest modern day equivalent. They are not bringing forth a new mammoth yet either—all of their work is confined to simple cells in their lab. What they have done, however, is build healthy living elephant cells with mammoth DNA in them. Their work is yet another step towards that ultimate goal, realizing the birth of a wooly mammoth that is as faithful to the original as is humanly possible.

Talk of cloning a mammoth began not long after scientists learned how to actually do cloning—mammoth carcasses have been found in very cold places which preserved remains, which of course, included DNA. But not everyone has been onboard with the idea—some claim it is stepping into God's territory, others suggest it seems ridiculous considering all of the species that are nearing extinction, including those of elephants. Why not use those financial resources that are now going towards bringing back something that has gone extinct, to saving those that are still here?

The technique the team is using is called Crispr, it allows for reproducing exact copies of genes—in this case 14 mammoth genes, which are then inserted into elephant genes. As Church explains, the team prioritizes which genes are replicated and inserted, based on such factors as hairiness, ear size, and subcutaneous fat, which the animal needed to survive in its harsh cold environment.

Not clear as yet is when or if the team at Harvard has plans to produce an actual living mammoth, or if they will leave that to other teams working on similar projects.

What these researchers tend to achieve is amazing. The woolly mammoth is the great ancestors of the modern elephants and was a magnificent mammal. To bring to like a reasonable facsimile is an extraordinary task. Personally I would love to pursue a career as a researcher and in the future I hope technology helps to further improve the work of researchers.

Before dinosaurs came along, one of Earth’s top predators was a salamander-like amphibian that lived in tropical areas of the supercontinent Pangaea. Fossils unearthed from a 30- to 40-centimeter-thick bone bed in southern Portugal suggest the creature was more than 2 meters long, weighed as much as 100 kilograms, and had a broad flat head the size and shape of a toilet seat. The newly described species (artist's representation shown), which lived between 220 million and 230 million years ago, was one of the largest in a group of amphibians known as metoposaurs and is the first known in this region from well-preserved fossils, the researchers report online today in the Journal of Vertebrate Paleontology.

The species has been dubbed Metoposaurus algarvensis to honor the Algarve region of Portugal, where the fossils were unearthed. (Even though the genus name contains the Greek word saur, which translates as “lizard,” these creatures and their kin were amphibians.) The 4-square-meter area of the bone bed already excavated has yielded 10 skulls and hundreds of remains, suggesting that the creatures became concentrated in one area and then died when the lake they inhabited dried up, the researchers say. Because the beasts had spindly limbs probably insufficient to support their weight, they likely remained in the water most of the time, feeding on fish but possibly snacking on small ancestors of dinosaurs or mammals that wandered too near the waterside. Similar bone beds that include other species of metoposaurs have been found in what are now Africa, Europe, and North America—a hint that climate at the time was highly unpredictable and prone to lengthy droughts.

Distasteful as it sounds, the transplantation of fecal matter is more successful for treating Clostridium difficile infections than previously thought. The research, published in the open access journal Microbiome, reveals that healthy changes to a patient's microbiome are sustained for up to 21 weeks after transplant, and has implications for the regulation of the treatment.

Clostridium difficile infections are a growing problem, leading to recurrent cases of diarrhea and severe abdominal pain, with thousands of fatalities worldwide every year. The infection is thought to work by overrunning the intestinal microbiome - the ecosystem of microorganisms that maintain a healthy intestine.

Fecal microbiota transplantation was developed as a method of treating C. difficile infection, and is particularly successful in patients who suffer repeat infections. Fecal matter is collected from a donor, purified, mixed with a saline solution and placed in a patient, usually by colonoscopy.

Previous research has shown that the fecal microbiota of patients resembles that of the donor, but not much is known about the short and long term stability of fecal microbiota transplanted into recipients.

In this research, Michael Sadowsky and colleagues at the University of Minnesota collected fecal samples from four patients before and after their fecal transplants. Three patients received freshly prepared microbiota from fecal matter and one patient received fecal microbiota that had previously been frozen. All received fecal microbiota from the same pre-qualified donor.

The team compared the pre- and post-transplant fecal microbial communities from the four patients, as well as from 10 additional patients with recurring C. difficile infections, to the sequences of normal subjects described in the Human Microbiome Project. In addition, they looked at the changes in fecal bacterial composition in recipients over time, and compared this to the changes observed within samples from the donor.

Surprisingly, after transplantation, patient samples appeared to sustain changes in their microbiome for up to 21 weeks and remained within the spectrum of fecal microbiota characterized as healthy.

By measuring a series of diffraction pattern from a virus injected into an XFEL beam, researchers at Stanford’s Linac Coherent Light Source (LCLS) have determined the first three-dimensional structure of a virus, using a mimivirus.

X-ray crystallography has solved the vast majority of the structures of proteins and other biomolecules. The success of the method relies on growing large crystals of the molecules, which isn’t possible for all molecules.

“Free-electron lasers provide femtosecond X-ray pulses with a peak brilliance ten billion times higher than any previously available X-ray source,” the researchers note in a paper inPhysical Review Letters. “Such a large jump in one physical quantity is very rare, and can have far reaching implications for several areas of science. It has been suggested that such pulses could outrun key damage processes and allow structure determination without the need for crystallization.”

The current resolution of the technique (about 100 nanometers) would be sufficient to image important pathogenic viruses like HIV, influenza and herpes, and further improvements may soon allow researchers to tackle the study of single proteins, the scientists say.

Mimivirus is one of the largest known viruses. The viral capsid is about 450 nanometers in diameter and is covered by a layer of thin fibres. A 3D structure of the viral capsid exists, but the 3D structure of the inside was previously unknown.

Herpes simplex virus infections are an enormous global health problem and there is currently no viable vaccine. For nearly three decades, immunologists’ efforts to develop a herpes vaccine have centered on exploiting a single protein found on the virus’s outer surface that is known to elicit robust production of antibodies. Breaking from this approach, Howard Hughes Medical Institute (HHMI) scientists at Albert Einstein College of Medicine have created a genetic mutant lacking that protein. The result is a powerfully effective vaccine against herpes viruses.

“We have a very promising new candidate for herpes,” says William Jacobs, an HHMI investigator at the Albert Einstein College of Medicine, “but this might also be a good candidate as a vaccine vector for other mucosal diseases, particularly HIV and tuberculosis.”

The new vaccine was found to be effective against the two most common forms of herpes that cause cold sores (HSV-1) and genital ulcers (HSV-2). Both are known to infect the body’s nerve cells, where the virus can lay dormant for years before symptoms reappear. The new vaccine is the first to prevent this type of latent infection. “With herpes sores you continually get them,” Jacobs says. “If our vaccine works in humans as it does in mice, administering it early in life could completely eliminate herpes latency.” Jacobs and his colleagues reported their findings on March 10, 2015, in the journal eLife.

HSV-2 is a lifelong, incurable infection that causes recurrent and painful genital sores and increases susceptibility to HIV. Also, babies born to mothers with active genital herpes have a more than 80 percent mortality rate. Current estimates suggest that 500 million people worldwide are infected with HSV-2, with approximately 20 million new cases occurring annually. While infection rates in the U.S. hover around 15 to 20 percent, HSV-2 is highly prevalent in sub-Saharan Africa, where nearly three in four women have contracted the virus, contributing significantly to the region’s HIV epidemic.

The related virus, HSV-1 is primarily associated with oral lesions, but is a major cause of corneal blindness and infects around 60 percent of the world’s population. Notably, HSV-1 has been increasingly recognized as a cause of genital herpes in the United States and other developed countries.

Scientists for decades have been worried about plastic clogging up our oceans, but now they finally know just how bad the problem is. We dump about five shopping bags full of plastic for every foot of coastline in the world every year, according to a new study. The numbers are orders of magnitude higher than prior estimates.

If we continue to produce large amounts of plastic—and can’t find a better way to dispose of them—the amount of plastic in our oceans will double over the next decade, according to Jenna Jambeck, an environmental engineer at the University of Georgia and lead author on the study.

She says these numbers actually undercount the problem because they account for only floating plastic. As much as 50 percent of the plastic produced in North America probably sinks to the ocean floor, she says.

The 8 million metric tons of plastic that litters our oceans every year consists of not only the usual suspects (like six-pack plastic rings, which are the bane of sea turtles), but also microplastics, tiny bits of debris smaller than your fingernail. Microplastics endanger marine life of all sizes, from whales to barnacles, as they are easy to swallow and may contain dangerous chemicals.

Jambeck and her team noticed at least one recurring theme within the data. Middle-income countries, especially those that have begun to industrialize but have not yet figured out how to manage their waste, end up tossing a lot of garbage in their oceans. One outlier is the United States, a rich country that would seem to have its waste management act together but still dumps a lot of plastic into the oceans.

A flatworm parasite called Ribeiroia ondatrae infects several species of frogs just as they're developing their limbs, causing an assortment of defects such as no legs or even multiple legs that jut out at weird angles from the frogs' bodies scientists say.

Watch a video of the deformed frogs.

The deformed frogs are often unable to move and either die or quickly get eaten by predators. Scientists already knew that the parasite was the culprit in the frog malformations, but the researchers wanted to find out whether known hot spots of Ribeiroia populations in four western states had changed since they were last surveyed in 1999. So in 2010 Pieter Johnson, an ecologist at the University of Colorado at Boulder, and colleagues gathered data on frogs and parasites in 48 wetlands in California, Oregon, Washington, and Montana.

The Ribeiroia parasite has a complex, multihost life cycle, which begins with the ramshorn snail, a creature common to many western U.S wetlands. The flatworm asexually clones itself inside the snail, stripping the mollusk of its gonads and converting it into a "parasite machine," Johnson said. Each night the snail releases hundreds of free-swimmingRibeiroia larvae, which seek out their next hosts—tadpoles—with "remarkable precision."

The parasite larvae penetrate the tadpoles' tissue and zero in on the developing limb buds, so that when a tadpole begins to metamorphose into a frog, its "primary system of locomotion doesn't work—it can't jump, can't swim," he said. "That's when the birds"—the parasite's final host—"zoom in and eat the young mutated frogs up like popcorn."

The parasite then reproduces sexually inside the birds, and when the birds defecate, their feces contain parasite eggs that eventually make their way back into the snails.

Though the Ribeiroia parasite occurs naturally in North America, human activities likely have something to do with its prevalence, Johnson noted. For instance, the snails feed on algae, and runoff from agriculture and industry into wetlands contains nutrients that act as fertilizer, boosting algae growth. With more snails in the wetlands, the parasites have more initial hosts to infect, Johnson noted.

Today, about one-tenth of the world’s population are southpaws. Why are such a small proportion of people left-handed -- and why does the trait exist in the first place? Daniel M. Abrams investigates how the uneven ratio of lefties and righties gives insight into a balance between competitive and cooperative pressures on human evolution.

Infusing liquids into polymers makes long lasting, self-replenishing material that repels deadly bacterial build-up. Harvard researchers have demonstrated a powerful, long-lasting, repellent surface technology that can be used with medical materials to prevent infections caused by microbial biofilms.

More than 80 percent of microbial infections in the human body are caused by a build-up of bacteria, according to the National Institutes of Health (NIH). Bacteria cells gain a foothold in the body by accumulating and forming into adhesive colonies called biofilms, which help them to thrive and survive but cause often serious infections and associated life-threatening risks to their human hosts. These biofilms commonly form on medical surfaces including those of mechanical heart valves, urinary catheters, intravenous catheters, and other implants. But a new study reported a powerful, long-lasting repellent surface technology that can be used with medical material to prevent these kind of infections caused by biofilms. The new approach, which its inventors are calling "liquid-infused polymers", joins an arsenal of slippery and hydrophobic surface coatings that have been developed at Harvard's School of Engineering and Applied Sciences (SEAS) and the Wyss Institute for Biologically Inspired Engineering.

Fourteen years ago, during the darkest moments of the “stem-cell wars” pitting American scientists against the White House of George W. Bush, one group of advocates could be counted on to urge research using cells from human embryos: parents of children with type 1 diabetes. Motivated by scientists who told them these cells would lead to amazing cures, they spent millions on TV ads, lobbying, and countless phone calls to Congress.

Now the first test of a type 1 diabetes treatment using stem cells has finally begun. In October, a San Diego man had two pouches of lab-grown pancreas cells, derived from human embryonic stem cells, inserted into his body through incisions in his back. Two other patients have since received the stand-in pancreas, engineered by a small San Diego company called ViaCyte.

It’s a significant step, partly because the ViaCyte study is only the third in the United States of any treatment based on embryonic stem cells. These cells, once removed from early-stage human embryos, can be grown in a lab dish and retain the ability to differentiate into any of the cells and tissue types in the body. One other study, since cancelled, treated several patients with spinal-cord injury (see “Geron Shuts Down Pioneering Stem-Cell Program” and “Stem-Cell Gamble”), while tests to transplant lab-grown retina cells into the eyes of people going blind are ongoing (see “Stem Cells Seem Safe in Treating Eye Disease”).

Douglas Melton, a biologist at Harvard University who has two children with type 1 diabetes, worries that the ViaCyte system may not work. He thinks deposits of fibrotic, scarlike tissue will glom onto the capsules, starving the cells inside of oxygen and blocking their ability to sense sugar and release insulin. Melton also thinks it might take immature cells up to three months to become fully functional. And many won’t become beta cells, winding up as other types of pancreatic cells instead.

Melton says the “inefficiency” of the system means the company “would need a device about the size of a DVD player” to have enough beta cells to effectively treat diabetes. ViaCyte says it thinks 300 million of its cells, or about eight of its capsules, would be enough. (Each capsule holds a volume of cells smaller than one M&M candy.) Last October, Melton’s group announced it had managed to grow fully mature, functional beta cells in the lab, a scientific first that took more than 10 years of trial-and-error research. Melton thinks implanting mature cells would allow a bioartificial pancreas to start working right away.

To encapsulate his cells, Melton has been working with bioengineer Daniel Anderson at MIT to develop their own capsule. Anderson doesn’t want to say exactly how it works, but a recent patent filing from his lab describes a container made of layers of hydrogels, some containing cells and others anti-inflammatory drugs to prevent the capsule from getting covered with fibrotic tissue. Both Melton and Anderson are cagey about discussing their results. “We do have some successes we are very excited about,” Anderson says. “The bottom line is we have reason to believe it is possible to use Doug’s cells in our devices and cure diabetes in animals.”

After the stem-cell wars, and then a decade of trying to turn the technology’s promises into reality, Henry says he feels convinced that “cells in bags” of some kind are going to be the answer to type 1 diabetes. He’s aware that curing rodents doesn’t guarantee the technology will help people, but he says the clinical trial he’s running is another in a series of “small steps” toward much-improved lives for millions of people. “I am just so positive that this is the future,” he says.

Researchers at North Carolina State University and the University of North Carolina at Chapel Hill have uncovered a novel approach to creating inhalable vaccines using nanoparticles that shows promise for targeting lung-specific diseases, such as influenza, pneumonia and tuberculosis.

The work, led by Cathy Fromen and Gregory Robbins, members of the DeSimone and Ting labs (see below), reveals that a particle’s surface charge plays a key role in eliciting immune responses in the lung. Using the Particle Replication in Nonwetting Templates (PRINT) technology invented in the DeSimone lab, Fromen and Robbins were able to specifically modify the surface charge of protein-loaded particles while avoiding disruption of other particle features, demonstrating PRINT’s unique ability to modify particle attributes independently from one another.

When delivered through the lung, particles with a positive surface charge were shown to induce antibody responses both locally in the lung and systemically in the body. In contrast, negatively charged particles of the same composition led to weaker, and in some cases undetectable, immune responses, suggesting that particle charge is an important consideration for pulmonary vaccination.

A paper describing the work, “Controlled analysis of nanoparticle charge on mucosal and systemic antibody responses following pulmonary immunization,” was published in the Proceedings of the National Academy of Sciences Dec. 29. The findings also have broad public health implications for improving the accessibility of vaccines. An inhalable vaccine may eliminate the need for refrigeration, which can not only improve shelf life, but also enable distribution of vaccines to low-resource areas, including many developing countries where there is significant need for better access to vaccines.

Unlike humans and great apes, rhesus monkeys don't realize when they look in a mirror that it is their own face looking back at them. But, according to a report in the Cell Press journal Current Biology on January 8, that doesn't mean they can't learn. What's more, once rhesus monkeys in the study developed mirror self-recognition, they continued to use mirrors spontaneously to explore parts of their bodies they normally don't see.

The discovery in monkeys sheds light on the neural basis of self-awareness in humans and other animals. "Our findings suggest that the monkey brain has the basic 'hardware' [for mirror self-recognition], but they need appropriate training to acquire the 'software' to achieve self-recognition," says Neng Gong of the Chinese Academy of Sciences.

In earlier studies, scientists had offered monkeys mirrors of different sizes and shapes for years, even beginning at a young age, Gong explains. While the monkeys could learn to use the mirrors as tools for observing other objects, they never showed any signs of self-recognition. When researchers marked the monkeys' faces and presented them with mirrors, they didn't touch or examine the spot or show any other self-directed behaviors in front of those mirrors in the way that even a very young person would do.

In the new study, Gong and his colleagues tried something else. They sat the monkeys in front of a mirror and shined a mildly irritating laser light on the monkeys' faces. After 2 to 5 weeks of the training, those monkeys had learned to touch face areas marked by a spot they couldn't feel in front of a mirror. They also noticed virtual face marks in mirroring video images on a screen. They had learned to pass the standard mark test for mirror self-recognition.

Scientists have compared for the first time the genomes of the two bacteria species that cause leprosy. The study shows how the two species evolved from a common ancestor around 13.9 million years ago, and offers new insights into their biology that could lead to new treatments.

Leprosy is a chronic infection of the skin, peripheral nerves, eyes and mucosa of the upper respiratory tract, affecting over a quarter million people worldwide. Its symptoms can be gruesome and devastating, as the bacteria reduce sensitivity in the body, resulting in skin lesions, nerve damage and disabilities. Until recently, leprosy was attributed to a single bacterium, Mycobacterium leprae; we now suspect that its close relative, Mycobacterium lepromatosis, might cause a rare but severe form of leprosy. EPFL scientists have analyzed for the first time the complete genome of M. lepromatosis, and compared it to that of the major leprosy-causing bacterium.

Published in PNAS, the study reveals the origin and evolutionary history of both bacteria, and offers new insights into their biology, global distribution, and possibly treatment. Along with its mutilating symptoms, leprosy also carries a stigma, turning patients into social outcasts. Although we have been able to push back the disease with antibiotics, leprosy remains endemic in many developing countries today.

Leprosy can manifest itself in various forms, all thought to be caused by the bacterium M. leprae. But in 2008, a study showed considerable evidence that another species of bacterium, M. lepromatosis, causes a distinct and aggressive form of the disease called “diffuse lepromatous leprosy”, found in Mexico and the Caribbean.

The lab of Stewart Cole at EPFL’s Global Health Institute carried out a genome-wide investigation on M. lepromatosis. This complex and computer-heavy technique looks at the bacterium’s entire DNA, locating its genes along the sequence. Because M. lepromatosis cannot be grown in the lab and animal models for this version of leprosy do not exist yet, the scientists used an infected skin sample from a patient in Mexico to obtain the bacterium’s genetic material.

After extracting the DNA from the entire sample, the researchers had to separate the bacterial DNA from the patient’s. To do this, they used two genetic techniques: one that increased the bacterium’s DNA and another that decreased the human DNA. With the bacterium’s DNA isolated, the researchers were able to sequence it and read it. Once they had the complete sequence of the bacterium’s genome, they were able to compare it with the known genome of M. leprae, the bacterium responsible for the majority of leprosy cases.

The study found that the two species of bacteria are very closely related. The comparative genomics analysis could “backtrack” the history of their genes, and showed that the two bacteria have diverged 13.9 million years ago from a common ancestor with a similar genome structure, and possibly a similar lifestyle. That ancestor suffered a process known as “gene decay”, where over a long period of time and multiple generations, a large number of genes mutated, became non-functional, and eventually disappeared. The study showed that the two new species continued to lose genes but from different regions of their genomes, indicating that during their evolution they occupied different biological roles and mechanisms to ensure survival.

SNARE proteins are known as the minimal machinery for membrane fusion. To induce membrane fusion, the proteins combine to form a SNARE complex in a four helical bundle, and NSF and α-SNAP disassemble the SNARE complex for reuse. In particular, NSF can bind an energy source molecule, adenosine triphosphate (ATP), and the ATP-bound NSF develops internal tension via cleavage of ATP. This process is used to exert great force on SNARE complexes, eventually pulling them apart. However, although about 30 years have passed since the Nobel Prize winners' discovery, how NSF/α-SNAP disassembled the SNARE complex remained a mystery to scientists due to a lack in methodology.

In a recent issue of Science, published on March 27, 2015, a research team, led by Tae-Young Yoon of the Department of Physics at the Korea Advanced Institute of Science and Technology (KAIST) and Reinhard Jahn of the Department of Neurobiology of the Max-Planck-Institute for Biophysical Chemistry, reports that NSF/α-SNAP disassemble a single SNARE complex using various single-molecule biophysical methods that allow them to monitor and manipulate individual protein complexes. "We have learned that NSF releases energy in a burst within 20 milliseconds to "tear" the SNARE complex apart in a one-step global unfolding reaction, which is immediately followed by the release of SNARE proteins," said Yoon.

Previously, it was believed that NSF disassembled a SNARE complex by unwinding it in a processive manner. Also, largely unexplained was how many cycles of ATP hydrolysis were required and how these cycles were connected to the disassembly of the SNARE complex.

Yoon added, "From our research, we found that NSF requires hydrolysis of ATPs that were already bound before it attached to the SNAREs--which means that only one round of an ATP turnover is sufficient for SNARE complex disassembly. Moreover, this is possible because NSF pulls a SNARE complex apart by building up the energy from individual ATPs and releasing it at once, yielding a "spring-loaded" mechanism."

NSF is a member of the ATPases associated with various cellular activities family (AAA+ ATPase), which is essential for many cellular functions such as DNA replication and protein degradation, membrane fusion, microtubule severing, peroxisome biogenesis, signal transduction, and the regulation of gene expression. This research has added valuable new insights and hints for studying AAA+ ATPase proteins, which are crucial for various living beings.

Reference: "Spring-loaded unraveling of a single SNARE complex by NSF in one round of ATP turnover." (DOI: 10.1126/science.aaa5267)

Scientists are using previously top-secret technology to zoom through the human body down to the level of a single cell. Scientists are also using cutting-edge microtome and MRI technology to examine how movement and weight bearing affects the movement of molecules within joints, exploring the relationship between blood, bone, lymphatics and muscle.

UNSW biomedical engineer Melissa Knothe Tate is using previously top-secret semiconductor technology to zoom through organs of the human body, down to the level of a single cell.

A world-first UNSW collaboration that uses previously top-secret technology to zoom through the human body down to the level of a single cell could be a game-changer for medicine, an international research conference in the United States has been told.

The imaging technology, developed by high-tech German optical and industrial measurement manufacturer Zeiss, was originally developed to scan silicon wafers for defects.

UNSW Professor Melissa Knothe Tate, the Paul Trainor Chair of Biomedical Engineering, is leading the project, which is using semiconductor technology to explore osteoporosis and osteoarthritis.

Using Google algorithms, Professor Knothe Tate -- an engineer and expert in cell biology and regenerative medicine -- is able to zoom in and out from the scale of the whole joint down to the cellular level "just as you would with Google Maps," reducing to "a matter of weeks analyses that once took 25 years to complete."

Her team is also using cutting-edge microtome and MRI technology to examine how movement and weight bearing affects the movement of molecules within joints, exploring the relationship between blood, bone, lymphatics and muscle. "For the first time we have the ability to go from the whole body down to how the cells are getting their nutrition and how this is all connected," said Professor Knothe Tate. "This could open the door to as yet unknown new therapies and preventions."

Professor Knothe Tate is the first to use the system in humans. She has forged a pioneering partnership with the US-based Cleveland Clinic, Brown and Stanford Universities, as well as Zeiss and Google to help crunch terabytes of data gathered from human hip studies. Similar research is underway at Harvard University and Heidelberg in Germany to map neural pathways and connections in the brains of mice.

The above story is based on materials provided by University of New South Wales.

The existence of ultra-small bacteria (aka “nanobacteria” or “nannobacteria”) has been debated for two decades, but there hasn’t been a comprehensive electron microscopy and DNA-based description of the microbes until now. They are about 200 nanometers (.2 micrometers) in width with a volume of only about 9 cubic nanometers. About 150 of these bacteria could fit inside an Escherichia coli bacteria cell.

The diverse bacteria were found in groundwater and are thought to be quite common. This is the smallest a cell can be and still accommodate enough material to sustain life, the researchers say. The bacterial cells have densely packed spirals that are probably DNA, a very small number of ribosomes, hair-like appendages, and a stripped-down metabolism that likely requires them to rely on other bacteria for many of life’s necessities.

“These newly described ultra-small bacteria are an example of a subset of the microbial life on earth that we know almost nothing about,” says Jill Banfield, a Senior Faculty Scientist in Berkeley Lab’s Earth Sciences Division and a UC Berkeley professor in the departments of Earth and Planetary Science and Environmental Science, Policy and Management.

“They’re enigmatic. These bacteria are detected in many environments and they probably play important roles in microbial communities and ecosystems. But we don’t yet fully understand what these ultra-small bacteria do,” says Banfield. To concentrate these cells in a sample, they filtered groundwater collected at Rifle, Colorado through successively smaller filters, down to 0.2 microns, which is the size used to sterilize water.

The frozen samples were transported to Berkeley Lab, where Birgit Luef, a former postdoctoral researcher in Banfield’s group characterized the cells’ size and internal structure using 2D and 3D cryogenic transmission electron microscopy. The images revealed dividing cells, indicating the bacteria were healthy and not starved to an abnormally small size.

The bacteria’s genomes were sequenced at the Joint Genome Institute, a DOE Office of Science User Facility located in Walnut Creek, California. The genomes were about one million base pairs in length.

Among their findings: Some of the bacteria have thread-like appendages, called pili, which could serve as “life support” connections to other microbes, and the bacteria lack many basic functions, so they likely rely on a community of microbes for critical resources.

Malaria is a serious disease that is estimated by the WHO to infect 200 million people a year, 600,000 of whom, primarily children under five, fatally. Malaria, which is most endemic in sub-Saharan Africa, is caused by different kinds of parasites from the plasmodium family, and effectively all cases of severe or fatal malaria come from the species known as Plasmodium falciparum. In severe cases of the disease, the infected red blood cells adhere excessively in the microvasculature and block the blood flow, causing oxygen deficiency and tissue damage that can lead to coma, brain damage and, eventually death. Scientists have therefore been keen to learn more about how this species of parasite makes the infected red blood cells so sticky.

It has long been known that people with blood type O are protected against severe malaria, while those with other types, such as A, often fall into a coma and die. Unpacking the mechanisms behind this has been one of the main goals of malaria research.

A team of scientists led from Karolinska Institutet in Sweden have now identified a new and important piece of the puzzle by describing the key part played by the RIFIN protein. Using data from different kinds of experiment on cell cultures and animals, they show how the Plasmodium falciparum parasite secretes RIFIN, and how the protein makes its way to the surface of the blood cell, where it acts like glue. The team also demonstrates how it bonds strongly with the surface of type A blood cells, but only weakly to type O.

Principal investigator Mats Wahlgren, a Professor at Karolinska Institutet's Department of Microbiology, Tumour and Cell Biology, describes the finding as "conceptually simple". However, since RIFIN is found in many different variants, it has taken the research team a lot of time to isolate exactly which variant is responsible for this mechanism.

"Our study ties together previous findings", said Professor Wahlgren. "We can explain the mechanism behind the protection that blood group O provides against severe malaria, which can, in turn, explain why the blood type is so common in the areas where malaria is common. In Nigeria, for instance, more than half of the population belongs to blood group O, which protects against malaria."

The advent and refinement of sequencing technologies has resulted in a decrease in both the cost and time needed to generate data on the entire sequence of the human genome. This has increased the accessibility of using whole-genome sequencing and whole-exome sequencing approaches for analysis in both the research and clinical contexts. The expectation is that more services based on these and other high-throughput technologies will become available to patients and the wider population. Some authors predict that sequencing will be performed once in a lifetime, namely, shortly after birth. The Public and Professional Policy Committee of the European Society of Human Genetics, the Human Genome Organization Committee on Ethics, Law and Society, the PHG Foundation and the P3G International Pediatric Platform address herein the important issues and challenges surrounding the potential use of sequencing technologies in publicly funded newborn screening (NBS) programs. This statement presents the relevant issues and culminates in a set of recommendations to help inform and guide scientists and clinicians, as well as policy makers regarding the necessary considerations for the use of genome sequencing technologies and approaches in NBS programs. The primary objective of NBS should be the targeted analysis and identification of gene variants conferring a high risk of preventable or treatable conditions, for which treatment has to start in the newborn period or in early childhood.

The development of next-generation sequencing (NGS) technologies has substantially reduced both the cost and the time required to sequence an entire human genome. The prospect of the availability of NGS technologies and consequently the greater facility to conduct whole-genome sequencing (WGS) have led some to predict that the use of this technology will change the current practice of medicine and public health by enabling more accurate, sophisticated and cost-effective genetic testing.1 It is anticipated that in the short term, the implementation of WGS in the clinic will improve diagnosis and management of some disorders with a strong heritable component,2 as well as improve personalized diagnosis and personalized drug therapy and treatment.

Presently, NGS is being used for targeted sequencing of sets of genes to help guide cancer treatment, and a number of cancer centers are considering using WGS or whole-exome sequencing (WES) in the future. During pregnancy, noninvasive prenatal testing for aneuploidy is also being done using NGS.3 In the clinic, WGS and WES are also being used to identify the causes of rare genetic diseases especially in children4 and in individuals with ‘atypical manifestations, (that) are difficult to confirm using clinical or laboratory criteria alone, or otherwise require extensive or costly evaluation’.5 Disorders for which WGS has been used as a diagnostic tool are usually genetically heterogeneous and have variable phenotypic expression such as intellectual disability, congenital malformations and mitochondrial dysfunctions.5 Other foreseen applications include tissue matching, disease risk predictions, reproductive risk information, forensics or even recreational genomic information (such as genealogy or nonmedically related traits).

Nonetheless, Goldenberg and Sharp6 predict that ‘it is likely that the earliest applications of whole-genome sequencing will be restricted to settings in which genetic testing is already a routine part of clinical or public health practice, such as state newborn screening (NBS) programs’.6 In truth, it should be noted that DNA testing, per se, is not a routine part of NBS and that only a very small proportion of babies, depending on the country, have a DNA test (as opposed to a biochemical test).7

Furthermore, the above prediction could be criticized as the routine nature of NBS with its often implied consent, together with its public health context, and the particular vulnerability of the population tested, would make it an unsuitable context into which to first welcome a WGS approach.

The microbes that call the New York City subway system home are mostly harmless, but include samples of disease-causing bacteria that are resistant to drugs — and even DNA fragments associated with anthrax and Bubonic plague — according to a citywide microbiome map published today by Weill Cornell Medical College investigators.

The study, published in Cell Systems, demonstrates that it is possible and useful to develop a "pathogen map" — dubbed a "PathoMap" — of a city, with the heavily traveled subway a proxy for New York's population. It is a baseline assessment, and repeated sampling could be used for long-term, accurate disease surveillance, bioterrorism threat mitigation, and large scale health management for New York, says the study's senior investigator, Dr. Christopher E. Mason, an assistant professor in Weill Cornell's Department of Physiology and Biophysics and in the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Al-Saud Institute for Computational Biomedicine (ICB).

The PathoMap findings are generally reassuring, indicating no need to avoid the subway system or use protective gloves, Dr. Mason says. The majority of the 637 known bacterial, viral, fungal and animal species he and his co-authors detected were non-pathogenic and represent normal bacteria present on human skin and human body. Culture experiments revealed that all subway sites tested possess live bacteria.

Strikingly, about half of the sequences of DNA they collected could not be identified — they did not match any organism known to the National Center for Biotechnology Information or the Centers for Disease Control and Prevention. These represent organisms that New Yorkers touch every day, but were uncharacterized and undiscovered until this study. The findings underscore the vast potential for scientific exploration that is still largely untapped and yet right under scientists' fingertips.

"Our data show evidence that most bacteria in these densely populated, highly trafficked transit areas are neutral to human health, and much of it is commonly found on the skin or in the gastrointestinal tract," Dr. Mason says. "These bacteria may even be helpful, since they can out-compete any dangerous bacteria."

But the researchers also say that 12 percent of the bacteria species they sampled showed some association with disease. For example, live, antibiotic-resistant bacteria were present in 27 percent of the samples they collected. And they detected two samples with DNA fragments of Bacillus anthracis (anthrax), and three samples with a plasmid associated with Yersinia pestis (Bubonic plague) — both at very low levels. Notably, the presence of these DNA fragments do not indicate that they are alive, and culture experiments showed no evidence of them being alive.

Yet these apparently virulent organisms are not linked to widespread sickness or disease, Dr. Mason says. "They are instead likely just the co-habitants of any shared urban infrastructure and city, but wider testing is needed to confirm this."

IF YOU must preserve messages for people in the far future to read, Blu-ray discs and USB sticks are no good. For real long-term storage, you want a DNA time capsule. Just 1 gram of DNA is theoretically capable of holding 455 exabytes – enough for all the data held by Google, Facebook and every other major tech company, with room to spare. It's also incredibly durable: DNA has been extracted and sequenced from 700,000-year-old horse bones. But conditions have to be right for it to last.

"We know that if you just store it lying around, you lose information," saysRobert Grass of the Swiss Federal Institute of Technology in Zurich. So he and colleagues are working on ways to increase DNA's longevity, with the aim of storing data for thousands or millions of years.

They began by looking at the way information is encoded on a DNA strand. The simplest method treats the DNA bases A and C as a "0" and G and T as a "1". Of course, any damage to the DNA leaves holes in the data, so the team used an error-correcting technique called a Reed-Solomon code. This includes redundant blocks that can be used to reconstruct garbled bits of data.

They also tried to mimic the way fossils keep a DNA sequence intact. Excluding all water from the environment was key, so they encapsulated the DNA in microscopic spheres of glass.

To test how long this storage system might last, they encoded two venerable documents, totalling 83 kilobytes: the Swiss federal charter from 1291, and the Archimedes Palimpsest, a 10th-century version of ancient Greek texts. DNA versions of these texts were kept at 60, 65 and 70 °C for a week to simulate ageing. They remained readable without any errors (Angewandte Chemie,doi.org/f23gmf).

The results suggest that data in DNA form could last 2000 years if kept at a temperature of around 10 °C. The Global Seed Vault in the Arctic could preserve it for over 2 million years at a chilly -18 °C, offering truly long-term storage.

Living deep underground ain't easy. In addition to hellish temperatures and pressures, there's not a lot to eat. Which is why oil reservoirs are the microbes’ cornucopia in this hidden realm.

Microbes feast on many oil reservoirs, but it has been unclear how the micro-organisms got to those locales. One proposal has been that the microbes colonize a pool of dead algae corpses and then go along for the ride as the pool gets buried deeper and deeper and the algae slowly become oil. That’s the so-called "burial and isolation" hypothesis.

But under that set of rules each pool of oil should have its own unique microbes—and that's not the case, according to a recent study in the Journal of the International Society for Microbial Ecology. [Camilla L. Nesbø et al, Evidence for extensive gene flow and Thermotoga subpopulations in subsurface and marine environments]

Researchers surveyed the genetics of oil-eating microbes from around the world. They found that populations from Nevada to the North Sea matched up almost exactly. They also determined that microbes in the North Sea appear to have swapped genes with Japanese microbes despite the locations being more than 8,000 kilometers apart on the Earth’s surface.

These findings suggest that the deep biosphere is actually filled with connections, and that microbes move from one oil reservoir to another, colonizing them almost as soon as they form in some cases. Or it could also be that marine microbes migrate down and then evolutionary selection pressure causes a convergence in the genetics that make it possible to survive under these extreme conditions.

Scientists have discovered a powerful new antibiotic they say can kill an array of germs without the bugs easily becoming resistant to it, a potential weapon against a range of diseases.

The discovery is a rare—and much-needed—breakthrough in the quest for new antibiotics to overcome the problem of growing resistance to existing drugs. While the new compound was shown to be safe and effective in mice, scientists need to determine whether this is the case for people.

The discovery of the new class of antibiotic, called teixobactin, was reported Wednesday in the journal Nature. It was uncovered by screening 10,000 bacterial strains from soil. Teixobactin will be investigated further in animals before being tested in people.

If all goes well, “we’ll be in clinical trials two years from now,” said Kim Lewis, a professorat Northeastern University in Boston and lead author of the study. Human trials could take two to three years, he added.

Because of widespread and indiscriminate use of antibiotics, bacteria in recent years have acquired mutations and new genes that render them more resistant to drugs. At the same time, antibiotic research at pharmaceutical companies stalled. This dual problem—the rise of resistant bacterial strains and the lack of new antibiotics—threatens to undermine many advances of modern medicine. Infections are becoming harder to control; standard treatments are less effective; illness and hospital stays are getting longer; and there are more deaths from infection.

Paralysed patients have been given new hope of recovery after rats with severe spinal injuries walked again through a ‘groundbreaking’ new cyborg-style implant. In technology which could have come straight out of a science fiction novel or Hollwood movie, French scientists have created a thin prosthetic ribbon, embedded with electrodes, which lies along the spinal cord and delivers electrical impulses and drugs.

The prosthetic, described by British experts as ‘quite remarkable’, is soft enough to bend with tissue surrounding the backbone to avoid discomfort.

Paralysed rats who were fitted with the implant were able to walk on their own again after just a few weeks of training. Researchers at the Ecole Polytechnique Fédérale de Lausanne are hoping to move to clinical trials in humans soon. They believe that a device could last 10 years in humans before needing to be replaced.

The implant, called ‘e-Dura’, is so effective because it mimics the soft tissue around the spine – known as the dura mater – so that the body does not reject its presence. “Our e-Dura implant can remain for a long period of time on the spinal cord or cortex,” said Professor Stéphanie Lacour.

“This opens up new therapeutic possibilities for patients suffering from neurological trauma or disorders, particularly individuals who have become paralyzed following spinal cord injury.” Previous experiments had shown that chemicals and electrodes implanted in the spine could take on the role of the brain and stimulate nerves, causing the rats' legs to move involuntarily when they were placed on a treadmill.

However the new gadget is flexible and stretchy enough that it can be placed directly onto the spinal cord. It closely imitates the mechanical properties of living tissue, and can simultaneously deliver electric impulses and drugs which activate cells. The implant is made of silicon and covered with gold electric conducting tracks that can be pulled and stretched. The electrodes are made of silicon and platinum microbeads which can also bend in any direction without breaking.

Most of the multiple sclerosis (MS) patients who took part in the cutting-edge stem cell study HALT-MS are still in remission years later. The phase 2 study has demonstrated impressive results by rebuilding the immune system using a patient’s own stem cells.

Studying 24 study volunteers who underwent stem cell transplants between 2006 and 2010, Dr. Richard A. Nash of the Colorado Blood Cancer Institute in Denver and his colleagues recently published their findings in JAMA Neurology. Researchers found that more than 86 percent of the patients remained relapse free after three years, and nearly 91 percent showed no sign of disease progression.

The goal was to reboot the patients’ immune systems. The researchers gauged success based on how long the patients remained relapse-free. The study involved patients with relapsing-remitting MS whose disease did not respond to at least one FDA-approved disease-modifying drug. Patients also had to score between 3.0 and 5.5 on the Expanded Disability Status Scale (EDSS), a set of tests to measure walking, cognition, dexterity, and quality of life in MS patients. People who fall into this range typically have mild to moderate disability.

Patients were given high-dose immunosuppressive therapy, or HDIT, to erase their native immune system. Then, researchers reintroduced blood-forming stem cells that had been harvested from the patients’ own blood.

“On average patients were hospitalized for three to four weeks,” said Nash in an interview with Healthline. That allowed enough time for the immune system to regenerate so patients could safely return home. “Patients are immunosuppressed, so they are on prophylactic antimicrobial medications. They are also educated regarding how to reduce the risk of infections after transplant,” explained Nash.

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